Starch and β-glucan in a whole-grain-like structural form improve hepatic insulin sensitivity in diet-induced obese mice

被引:16
作者
Luo, Kaiyun [1 ]
Wang, Xufeng [2 ]
Zhang, Genyi [1 ]
机构
[1] Jiangnan Univ, Sch Food Sci & Technol, Key Lab Food Sci & Technol, 1800 Lihu Ave, Wuxi 214122, Jiangsu, Peoples R China
[2] Fuzhou Univ, Coll Biol Sci & Engn, Inst Biotechnol, 523 Gongye Rd, Fuzhou 350002, Fujian, Peoples R China
基金
中国国家自然科学基金;
关键词
FATTY LIVER; NUTRITIONAL PROPERTY; CELL-FUNCTION; RESISTANCE; GLUCOSE; MECHANISMS; INFLAMMATION; MICROBIOTA; DISEASE; PROTEIN;
D O I
10.1039/c9fo00798a
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Whole-grain food (WGF) is well known for its anti-diabetic effect, and alleviation of obesity-induced insulin resistance (IR) might be one of the underlying mechanisms. In the current study, the effects of starch, as the main component in WGF, and beta-glucan in a whole-grain-like structural form (WGLSF) on hepatic IR and glucose homeostasis were investigated using high-fat (HF)-induced obese C57BL/6J mice. After treatment for 8 weeks, the body weight gain and IR of the mice were significantly reduced. The hepatic Akt, the key component in insulin signaling, was activated, and the hepatic expression and protein levels of glucose-6-phosphatase (G-6-P) and phosphoenolpyruvate carboxykinase (PEPCK) were reduced. Moreover, WGLSF effectively reduced the hepatic levels of free fatty acids and the pro-inflammatory cytokines TNF-alpha, IL-6, and NF-kappa B. Additionally, the reduced level of the phosphorylated c-Jun-N-terminal kinases (JNK) indicated that WGLSF treatment might inactivate the JNK signaling, leading to improved hepatic IR. These results demonstrated that starch and beta-glucan in a whole grain-like structural form have the potential as a dietary strategy to combat obesity-induced hepatic IR for improved health.
引用
收藏
页码:5091 / 5101
页数:11
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